SARS-CoV-2: Male Fertility
Impact of COVID-19 on male reproductive functions and need in-depth research for the exact underlying mechanisms how COVID-19 is associated with men’s health and fertility.
SARS-CoV-2 causing the COVID-19 has been declared a pandemic by the WHO on 11th March 2020. Now more than 2.5 million COVID-19 cases in world wide.
A huge research on this virus are carried out to reveal the fact of its multivariate pathology. Surprisingly, man are reported more affected to COVID-19 even with higher fatality rate compared to women.
Thus, it is an important to determine whether SARS-CoV-2 infection can even affect male fertility as an immediate or long-term consequence of the disease.
A number of data available, a crucial finding is that Angiotensin Converting Enzymes 2 (ACE2) receptor, that are the entry point of SARS-CoV-2 into host cells, is also rich in testicular cells.
In addition, the endogenous Androgen Milieu and its receptors are associated with ACE2 activation reflecting that enhanced Testosterone levels may trigger the Pathogenesis of COVID-19.
Moreover, SARS-CoV-2 infection-induced uncontrolled inflammatory responses may lead to systemic Oxidative Stress (OS), where severe disruptive effects on testicular functions.
Role of SARS-CoV-2:
ACE2 receptor plays a key role in the COVID-19 pathogenesis aiding direct host cell damage.
In male fertility research that tests show almost the highest ACE2 mRNA and protein expression among the various body tissues.
The four main testicular cell types showing expression of ACE2 mRNA are the-
1. Seminiferous duct cells
3. Leydig cells
4. Sertoli cells
Moreover, distinctly high ACE2 expression in testicular cells, while comparatively low expression levels of ACE2 in Ovarian cells, may also support higher vulnerability of SARS-CoV-2 mediated impairment in male gonadal functions.
Testicular expression of ACE2 has been shown to be age-based. The highest expression in patients aged 30 and older than 20 has been reported , whereas, those aged 60 have the lowest expression levels.
That could show that young patients are more likely than older patients to experience testicular injury due to COVID-19.
Mechanisms of SARS-CoV-2:
The first step needed of SARS-CoV-2 infectivity is the Proteases-mediated priming of its spike Proteins with host cell receptor, mainly via the transmembrane protease, Serine2 (TMPRSS2).
TMPRSS2 have been suggested to cleave ACE2 receptor aiding the entry of the virus into host cell.
Evidences claim that Androgen Receptor activation is needed to trigger TMPRSS2 gene transcription.
Since, gene loci of Androgen receptor and ACE2 are located in Chromosome X, increased X-linked inheritance of genetic polymorphisms and consequently endogenous Androgen actions may be a possible mechanism to explain male vulnerability to COVID-19.
So, at the last we can say that this possibility needs to be investigated through follow-up studies of the reproductive functions of reclaimed male patients. Thus, it can’t be ruled out that COVID-19 could have immediate or delayed impacts on male fertility status.
It is a crucial to undertake through research to reveal the exact impact and mechanism by which the COVID-19 might affect the male fertility.